Pyrrolizidine alkaloidosis

Pyrrolizidine alkaloidosis is a disease caused by chronic poisoning found in humans and other animals caused by ingesting poisonous plants which contain the natural chemical compounds known as pyrrolizidine alkaloids.[1] Pyrrolizidine alkaloidosis can result in damage to the liver, kidneys, heart, brain, smooth muscles, lungs, DNA, lesions all over the body, and could be a potential cause of cancer.[1][2] Pyrrolizidine alkaloidosis is known by many other names such as "Pictow Disease" in Canada and "Winton Disease" in New Zealand.[3] Cereal crops and forage crops can sometimes become polluted with pyrrolizidine-containing seeds, resulting in the alkaloids contaminating flour and other foods, including milk from cows feeding on these plants.[4][5]

Plant types and causes

Pyrrolizidine alkaloidosis is caused by the consumption of one or more of the 200 known plant species containing the toxic pyrrolizine alkaloids found all over the world today.[3] Established as the most common source of this illness are plants such as ragwort (Senecio jacobaea), woolly groundsels (Senecio redellii, Senecio longilobus), rattleweed (Crotalaria retusa), and seeds of yellow tarweed (Amsinckia intermedia).[1] There are 30 known pyrrolizidine alkaloids that are hepatotoxic, meaning they cause injury to the liver.[2] Although animals innately know to give these toxic plants a wide berth while grazing, in extreme drought conditions animals have been known to ingest them as a source of minimal protein. Animals can also be poisoned if the toxic plant material is in pellets, or harvested with grain.[1][6]

Frequency and exposure

Humans

Pyrrolizidine alkaloidosis poisoning in the United States has remained moderately rare among humans. The most common reports are the outcome of the misuse of medicinal home remedies, or the alkaloids are present in food and drink substances such as milk and honey when the animal carriers were exposed to the toxins. In other countries, mass human poisonings have occurred when cereal crops used were infected with seeds containing pyrrolizidine alkaloids.[4][7][8][9]

Infants and young children are most likely to acquire pyrrolizidine alkaloidosis because of their intrinsic nature to put everything they find into their mouths. However, anyone who consumes one of the mentioned toxic plants is susceptible to the disease.[7]

The typical case of pyrrolizidine alkaloidosis toxicity ends in liver damage that ranges from severe to moderate, as well as damage to other organs. The longevity of the disease is wide ranging from 2 weeks to 2 years subsequent to when the poison was ingested. The patient's recovery results may be as diverse as the permanence. Some have recovered as if they were never affected by pyrrolizidine alkaloidosis poisoning if the damage to the liver was not too severe, and others have died from it.[4]

The severity of pyrrolizidine alkaloidosis depends on how much of the poisonous plant was consumed in a height, age, and weight to the amount of substance ingested ratio. The only difference in the symptoms will be how prominent they are depending on the above ratio. Symptoms include:[2][4][7][10]

To stop the spread and severity of pyrrolizidine alkaloidosis the first step is to remove the poisonous plant from the source. Once the plant has been removed, the alkaloids can be extracted with chloroform. However, ethyl acetate is a handy and less toxic substitute.[2] Depending on the severity of the toxicity and how long the person has been exposed to the disease, there may be no means of treatment and fatality may occur.

Prevention

The only known technique of prevention is to avoid ingesting the poisonous alkaloids. Some methods of control have been defoliation in areas in both Oregon and California. Also mass relocation efforts of moths, flea beetles and seed flies have been made in hopes that they will eat the toxic plants and help control the population of the plants. This manner of alkaloid control has been met with variable success. Because sheep and goats have such a high immunity to the toxicity of the alkaloids they are commonly used to graze on the plants to control them. However, this method has its risks unless sheep meant for early slaughter are used. Before hay cutting in the spring is the optimal time frame for annual herbicide applications which have also enhanced the destruction of the alkaloids.[1][7][11]

References

  1. 1 2 3 4 5 The Merck Veterinary Manual. Pyrrolizidine Alkaloidosis: Introduction (Seneciosis, Senecio poisoning, Ragwort toxicity). Merck & Co., Inc., 2008. Web. 15 November
  2. 1 2 3 4 Rizk, Abdel-Fattah M., Naturally Occurring Pyrrolizidine Alkaloids. Doah: CRC Press, 1990
  3. 1 2 Hirono, I. Naturally Occurring Carcinogens of Plant Origin. Toyoake: Elsevier, 1987
  4. 1 2 3 4 Bad Bug Book. Pyrrolizidine Alkaloids. U.S. Food & Drug Administration, 17 Sep, 1998. Web. 3 November
  5. ↑ Dharmananda, Ubhuti. Safety Issues Concerning Herbs: Pyrrolizidine Alkaloids. Institute for Traditional Medicine, 2007. Web. 5 November
  6. ↑ Talcott P: Pyrrolizidine Alkaloid Poisoning. In: Robinson NE (ed): Current Therapy in Equine Medicine, 5th Edition. Philadelphia, W.B. Saunders Co., 2003, pp. 788-790
  7. 1 2 3 4 World Health Organization, Environmental Health Criteria 80. Geneva: World Health Organization, 1988
  8. ↑ Culvenor, C.C., Edgar J.A. Smith L.W., "Pubmed." Pyrrolizidine Alkaloids in honey from Echium Plantagineum L. USA.gov, 2009. Web. 17 September
  9. ↑ Magnuson, Bernadene. "ExtoxNet FAQs" Pyrrolizidine Alkaloids. EXTOXNET FAQ Team, 1997. Web. 20 October
  10. ↑ Plant poisoning - Pyrrolizidine alkaloids, wrongdiagnosis.com
  11. ↑ Cheeke, P.R. Symposium on Pyrrolizidine (Senecio) Alkaloids: Toxicity, Metabolism, and Poisonous Plant Control Measures

External links

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